Markers of myocodial fibrosis in acute myocardial infarction

Abstract Funding Acknowledgements Type of funding sources: None. One the leading mechanisms in healing process acute myocardial infarction (AMI) is damage and loss extracellular matrix, which plays a role pathogenesis LV remodeling. Tissue inhibitor matrix metalloprotease-1 protein that natural metalloproteases, forms complexes with MMP-1 other metalloproteases (they destroy components heart), irreversibly inhibiting their activity. Bayes-Genis A. et al presented histological data on expression ruptured eroded plaques plasma A (PAPP-A), metalloproteinase insulin-like growth factor-1 detected during pregnancy. Myocardial formation aldosterone angiotensin II (as result activation renin-angiotensin-aldosterone system, including tissue component) after stimulates collagen fibrous myocardium further changes structure geometric characteristics left ventricle. Purpose study. To study markers interstitial fibrosis stage assess dynamics these indicators patients 2.5-3 weeks inpatient treatment. Methods. The included 31 ST segment elevation. control groups consisted 20 apparently healthy individuals. During study, serum parameters metalloproteinase-1 (TIMMP-1 were measured days 1-3 AMI Results. level TIMMP-1 MI was 418.19 ± 103.77 ng / ml statistically significantly higher than practically individuals - 103.44 7.06 (p <0.0001) , 3 weeks, against background ongoing therapy, 366.70 93.34 ml, decrease TIMMP-1, compared initial value stage, had statistical significance = 0.046). 165.12 32.67 pg group. In who are hospitalized, for there significant 0.003) concentration blood by 15.1% from to 140.24 22.78 ml. Conclusions. (1-3 days), increase concentrations fibrosis, such as aldosterone, reflects initiation fibroblast processes and, accordingly, stimulation synthesis. Subsequently, aldosterone.